Effect of Acute Liver Damage on Ac-Globulin Activity of Plasma

Sykes, Edwin M.; Seegers, Walter H.; Ware, Arnold G.

doi:10.3181/00379727-67-16355p

Cited by 25 publications

(6 citation statements)

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“…In addition, observations after hepatectomy (3,4) and hepatic injury (5,6) and in hepatic disease (7,8) have provided a body of evidence consistent with hepatic synthesis of fibrinogen, prothrombin, and Factors V, VII, IX, and X. This evidence, however, has not been considered definitive, mainly because it is based on indirect observations in vivo in humans and in animals suffering from variable, often profound, metabolic abnormalities induced by hepatic dysfunction or extirpation.…”

mentioning

confidence: 96%

Synthesis of clotting factors by the isolated perfused rat liver.

Olson¹,

Miller²,

Troup³

1966

J. Clin. Invest.

101

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The liver has been proposed as a site of synthesis of blood-clotting factors, in part because of the demonstrated dominant role of the liver in synthesis of all plasma protein fractions except the y-globulins (1, 2). In addition, observations after hepatectomy (3, 4) and hepatic injury (5, 6) and in hepatic disease (7,8) have provided a body of evidence consistent with hepatic synthesis of fibrinogen, prothrombin, and Factors V, VII, IX, and X. This evidence, however, has not been considered definitive, mainly because it is based on indirect observations in vivo in humans and in animals suffering from variable, often profound, metabolic abnormalities induced by hepatic dysfunction or extirpation.This report describes the use of the isolated perfused rat liver in a more direct experimental evaluation of the role of the liver in the production of blood-clotting factors. The use of the isolated perfused liver was encouraged by Lupton's observations of shortened prothrombin time during perfusions of 3 to 4 hours (9), and by Pool and Robinson's studies of changes in clotting factor activity during in vitro incubation of rat liver slices (10). Presented here is not only more detailed direct evidence of hepatic synthesis of prothrombin and Factor VII, but also the first direct evidence for hepatic synthesis of Factors V and X.

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confidence: 96%

Synthesis of clotting factors by the isolated perfused rat liver.

Olson¹,

Miller²,

Troup³

1966

J. Clin. Invest.

101

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“…Results were negative in all other tissues examined. The findings confirm the presence of factor V in hepatic parenchymal cells and support the suggestion that endothelial coagulation factors may play a role in haemostasis and thrombosis.Many studies have implicated the livcr as a site of storage or synthesis of factor V. Thus, hepatic damage caused by chloroform has been shown to reduce plasma factor-V levcls (Sykes et al, 1948) and clinical observations have dcmonstrated factor-V deficiency in patients with liver disease (Owren, 1949;Deutsch, 1965 ; Walls & Losowsky, 1971). Pool & Robiiison (19j9a) failed to demonstrate synthesis of factor V in culturcs of rat liver sliccs, although organ perfusion studies have suggested that the livcr is in fact a site of factor-V production (Olson et al, 1966).…”

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confidence: 99%

The Immunological Localization of Factor V in Human Tissue

1975

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Antibody to factor V was produced by immunizing rabbits with purified factor V from human plasma. Various tissues were examined for the presence of factor-V antigen using this antiserum. It was consistently demonstrated in homogenates of liver and spleen by means of an antibody (coagulation inhibitor) neutralization technique. The antigen was further localized histologically by the indirect fluorescent antiglobulin technique. It was present on the endothelium of normal blood vessels in all organs examined. In the liver it was detected in hepatic parenchymal cells and a distinctive pattern of fluorescence in the spleen suggested that it was being detected on platelets. Results were negative in all other tissues examined. The findings confirm the presence of factor V in hepatic parenchymal cells and support the suggestion that endothelial coagulation factors may play a role in haemostasis and thrombosis.

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“…The interval of storage required for the development of increased prothrombic activity varies widely. In some instances the change becomes evident within 24 or 48 hours; in others, two weeks or more are necessary (table I). When citrate (one part of 2.5 yO sodium citrate solution to 9 parts of blood) is used instead of oxalate as anticoagulant the appearance of hyperreactivity is delayed.…”

Section: Resultsmentioning

confidence: 99%

“…r Insufficiency of plasma AC-globulin has been induced in dogs by injuring the liver with chloroform, resulting in an elevated prothrombin time (24). Why hypereactivity does not occur in plasma stored at room or body temperature in contrast to refrigerator temperature is obscure.…”

Section: Discussfonmentioning

confidence: 99%